Daniel's currently lying in a dark room with an aura crawling across his vision, and he used the last few minutes of usable eyesight to send us a question about what's happening inside his skull. That's either dedication or a very specific kind of procrastination.
He took paracetamol and everything. So while the shimmering lights do their thing, he wants to know what an aura actually is, why it sometimes comes with a pounding headache and sometimes doesn't, why auras vary so much between people, and why his migraines went from every few months as a teenager to once every few years now. Four questions, one brain wave.
I appreciate that he's using the episode as part of the recovery protocol. Lie down, take the painkiller, let two animals explain your neurology to you.
It's a legitimate medical intervention. Distraction reduces perceived pain intensity. Though I'm not sure our voices qualify as clinical-grade distraction.
Speak for yourself. My voice has been described as a weighted blanket made of sound.
By who?
Me. Just now. Anyway, let's get into this because the aura is one of the strangest things a human brain can do. Daniel describes it as a shimmering multicolored thing that obscures his vision. That's the classic presentation. And the mechanism behind it is wilder than the symptom.
It really is. So here's the core of it. What Daniel is experiencing right now is something called cortical spreading depression. CSD for short. It's a wave of intense electrical activity that sweeps across the surface of the brain at about two to five millimeters per minute. Neurons fire massively, then go silent. The wave moves, and as it moves, it drags a period of suppressed brain activity behind it.
Two to five millimeters per minute. That's... slow. Like a weather front crossing a map.
That's exactly the right image. And because it's slow and it follows the geography of the cortex, you can actually watch your own aura move. The shimmering crescent that starts near the center of your vision and expands outward over several minutes is the wave marching across your occipital cortex, which is the visual processing area at the back of your head.
So the shape Daniel sees is literally a map of his brain's surface, drawn in light.
Yeah. The visual cortex is organized spatially, it has a map of your visual field. As the wave crosses that map, the part of your vision corresponding to the neurons being depolarized starts to flicker and distort. Then when the wave passes and those neurons go quiet, you get a blind spot in that area. The shimmering edge is the wavefront. The darkness behind it is the depression.
That's the part that always struck me as eerie. You're not seeing a problem with your eyes. Your visual cortex is being short-circuited, and your brain is showing you the short circuit in real time.
There's a beautiful historical detail here. A psychologist named Karl Lashley in the nineteen forties suffered from migraines with aura himself. He carefully documented his own visual auras, measured how fast the shimmering edge moved across his visual field, and calculated that whatever was happening in his brain was propagating at about three millimeters per minute. He published that. Then a Brazilian physiologist named Aristides Leão had already described this exact wave in rabbit brains in nineteen forty-four. The speeds matched. Lashley had essentially measured his own cortical spreading depression from the inside, just by watching his aura.
So the man used his own migraine as a scientific instrument. That's remarkable. And it means the aura isn't just a symptom, it's a direct readout of a physical process. You can time it with a stopwatch.
And people have. The wave starts at the back of the brain, in the occipital cortex, which is why visual symptoms almost always come first. Then it can spread forward. If it reaches the somatosensory cortex, the part that processes touch, you get tingling or numbness, usually starting in the fingers and moving up the arm, sometimes into the face. If it reaches language areas, you get difficulty speaking or finding words. That's why auras can be so different between people. It depends entirely on which neighborhoods of the brain the wave rolls through.
So Daniel's visual aura, his coworker's sensory version, someone else's aphasia, those are all the same event, just at different addresses.
Right. And the percentages bear this out. Visual aura is by far the most common, over ninety percent of people with migraine with aura get visual symptoms. Somatosensory aura, the tingling and numbness, shows up in about thirty to thirty-six percent. Speech and language symptoms in about fourteen to twenty percent. And there are rarer forms, brainstem aura with vertigo, double vision, ringing in the ears, even decreased consciousness. Hemiplegic migraine where you get actual weakness on one side of the body, that's about one in ten thousand.
One in ten thousand. So when someone says their migraine makes their arm go weak, that's not them being dramatic. That's a specific, terrifying variant.
And it runs in families. Hemiplegic migraine has known genetic mutations, ion channel genes, which tells you something about the underlying mechanism. These are disorders of neuronal excitability. The brain is primed to fire off a spreading wave under certain conditions.
Let me ask the obvious question then. Why does this wave happen at all? What sets it off?
That's the part where I have to be honest about the limits of what we know. The initiation of cortical spreading depression requires a local buildup of extracellular potassium above a certain threshold, roughly twelve millimolar. When enough neurons in a small area depolarize, they dump potassium into the surrounding space. If the concentration gets high enough, it triggers neighboring neurons to depolarize, which releases more potassium, and the wave becomes self-sustaining. It's like a forest fire where the heat from one tree ignites the next.
And what lights the first tree?
That's the mystery. We know the threshold, we know the propagation mechanism, but why a particular brain on a particular Tuesday decides to cross that threshold is not fully understood. There are triggers, stress, sleep disruption, hormonal fluctuations, certain foods, flickering lights. But plenty of people with those triggers never get migraines, and plenty of migraine attacks happen with no obvious trigger at all.
So we understand the fire, but not the arsonist.
That's a fair summary. And it connects to something important. Migraine is a disorder of brain excitability. The brain of a migraineur is more prone to these waves than the brain of someone who doesn't get them. That susceptibility is partly genetic, partly hormonal, partly environmental. Estrogen is a huge factor, which is why migraine is about three times more common in women than men, and why attacks often track the menstrual cycle.
Daniel's a man, so the estrogen piece is less relevant to him personally. But the excitability piece is. His brain, at least during his teenage years, was more likely to tip into this state.
And that's a segue to his fourth question, which I want to get to properly. But first, let's tackle the thing he said seems odd. The visual disturbance and the headache seem like such different phenomena. Why do they travel together?
Right. You see lights for twenty minutes, then your head hurts for hours. On the surface, those have nothing to do with each other.
And this is where the science gets unsettled. The textbook story, the one I learned in medical school, is that the cortical spreading depression wave activates the trigeminal nerve, which is the main sensory nerve for the face and head. The trigeminal nerve innervates the meninges, the membranes around the brain. When the CSD wave reaches the meninges, it triggers the release of inflammatory peptides, particularly something called CGRP, calcitonin gene-related peptide. That causes blood vessels to dilate, creates neurogenic inflammation, and sensitizes pain pathways. The result is the throbbing, pounding headache.
So the wave rolls through the visual cortex, you get the shimmer. The wave reaches the meninges, triggers inflammation, you get pain. The delay between aura and headache is the time it takes for that inflammatory cascade to build.
That's the classic model. And there's animal evidence for it. Induce CSD in a rodent, and within an hour the animal shows signs of facial sensitivity, allodynia, that can be blocked with sumatriptan, a migraine drug. The timing matches the clinical lag between aura and headache. It's a coherent story.
But you said the science is unsettled. What's the problem?
The problem is that the new migraine drugs don't fit the story. The CGRP monoclonal antibodies, these are the big breakthrough of the last decade, work incredibly well for preventing migraine. They work for migraine with aura and migraine without aura. But they don't stop the aura itself. And these are large molecules that don't cross the blood-brain barrier well. So if they're working outside the brain, but the aura is happening inside the brain, and the drugs prevent the headache but not the aura, then maybe the aura isn't causing the headache at all.
Maybe both are triggered by something upstream, and the aura is a parallel event, not the cause.
There's a hypothesis that a common trigger, possibly in the hypothalamus or brainstem, sets off both the CSD wave and the headache pathway independently. The aura and the pain would then be siblings, not parent and child.
That would explain something Daniel mentioned. He occasionally managed to evade the migraine itself after having an aura. If the aura directly caused the headache, you'd expect the headache to follow every time. But if they're parallel processes, sometimes one fires without the other.
The numbers are striking. About thirty-eight to forty percent of people with migraine with aura have had at least one aura without a headache. About four percent of migraine patients exclusively get aura with no headache at all. That's called acephalgic migraine, or typical aura without headache.
Acephalgic. No head. The head pain is absent.
Right. And here's a fascinating detail. A survey of Norwegian neurologists found that thirty-four percent of them reported having experienced migraine aura without headache at least once. These are people trained to recognize the phenomenon. And standard screening questions for migraine usually start with, do you get headaches? So if you only get the aura, you might never be diagnosed. You might think you're having some weird eye problem or a transient neurological event.
Which is a shame, because the aura alone can be disabling. Daniel mentioned having to pull over his car because he couldn't see. That's not a minor inconvenience. That's a safety event.
And it's under-recognized. There are no clinical trials for treating isolated aura. The drugs we have target the headache. If your problem is purely the visual disturbance, there's very little evidence base for what to do about it.
Let me ask about the aura itself, because Daniel described his as shimmering and multicolored, and he noted that his coworker's experience was completely different. How much variety is there in the visual presentation alone?
A systematic review from last year catalogued twenty-five or twenty-six distinct elementary visual symptoms. Zigzag lines, blind spots, colored dots, tunnel vision, a heat wave distortion, things appearing too small or too large, a curtain effect where vision just gets wiped out from one side. Some people see a flickering crescent that expands. Some see a kaleidoscope. Some see black and white geometric patterns. Some see colors that aren't there.
And the positive symptoms, the lights and zigzags, tend to come first, then the negative symptoms, the blind spots, follow behind.
That's the wave. The leading edge is excitation, the trailing edge is suppression. You literally see the depolarization followed by the depression.
The condition names itself. Spreading depression. The depression is the silence after the storm.
And here's a detail that I find remarkable. People who are blind from eye disease or optic nerve damage can still experience visual aura. Because the aura isn't generated in the eyes. It's generated in the visual cortex. If the cortex is intact, the aura can happen, even if the eyes can't see anything at all. These patients report seeing lights and shapes despite having no functional vision.
That's the brain hallucinating its own architecture. The visual cortex is firing in a pattern that doesn't correspond to any incoming signal, and the brain interprets it as sight.
Which is also why the aura moves in a way that matches the cortical map. The visual field is represented in the brain in a distorted way, more cortex devoted to central vision than peripheral. The aura's movement reflects that distortion. Lashley used his own aura to map his visual cortex. He was essentially doing neuroanatomy by introspection.
Let me go back to something you said earlier. The wave moves at two to five millimeters per minute. Daniel's aura lasts, what, twenty minutes? Half an hour?
Typical visual aura lasts five to thirty minutes. The full aura complex, if it includes sensory and speech symptoms, can last up to an hour. That's the diagnostic window. If the symptoms last much longer than an hour, you start thinking about other things.
Like what?
Stroke, for one. Migraine with aura carries about a twofold increased risk of stroke, particularly in women who smoke and take oral contraceptives. The mechanisms aren't fully understood, but the vascular changes during CSD may play a role. It's not something to panic about, the absolute risk is still low, but it's a real association.
So if someone has a visual disturbance that lasts three hours, that's not a migraine aura. That's a different conversation.
Correct. The time course is diagnostic. Aura builds gradually over minutes, spreads, and resolves within an hour. A stroke or a transient ischemic attack typically hits suddenly and doesn't have that slow march. The marching quality is the signature of CSD.
Daniel's pattern is a slow build, the shimmer expanding, then it fades, then the headache arrives or doesn't. That's textbook.
And the fact that he sometimes dodges the headache entirely is not unusual. It's a recognized variant. His brain generates the wave, but the trigeminal system doesn't get sufficiently activated to produce pain. Why that happens in some attacks and not others, we don't have a good molecular answer for. It's one of the open questions in the field.
Let's talk about the natural history, because Daniel asked about that specifically. Teenage migraines every few months, then tapering off to once every few years. He wanted to know if that's a common pattern.
It's extremely common. And the epidemiology backs it up. Migraine prevalence rises during puberty, peaks between ages thirty-five and thirty-nine, and then declines with age. By the time people are in their seventies, the prevalence drops to under four percent.
So the peak is middle age, not adolescence. Daniel's experience of teenage migraines was the beginning of the curve, not the top.
Right. And here's the counterintuitive part. As people age, the headache intensity tends to diminish, but the aura symptoms, particularly visual ones, can become more pronounced. So you get this population of older people who stop having the pounding headaches but continue having visual auras, sometimes more frequently. They become aura-only migraineurs.
That's exactly Daniel's trajectory, just compressed. His headaches faded, but the aura still shows up occasionally. He's drifting toward the acephalgic end of the spectrum.
And the brainstem aura variant, the one with vertigo and double vision, that often starts in the teenage years and then diminishes in adult life, sometimes being replaced by other forms of migraine. One study found headache remission in about thirty-eight percent of brainstem aura patients, compared to twenty-three percent of all migraine with aura patients. So the pattern of adolescent onset followed by remission is well documented.
Why does the brain calm down with age?
Partly hormonal. Estrogen drops after menopause, and estrogen is a major modulator of CSD susceptibility. Partly it's just the natural history of the disorder. The brain's excitability set point shifts over the lifespan. We don't fully understand the mechanisms, but the pattern is consistent across populations.
Daniel also asked what migraines actually are. We've been talking about aura, but let's define the broader condition.
Migraine is a chronic neurological disorder characterized by recurrent attacks of headache, often with associated symptoms like nausea, sensitivity to light and sound, and in some people, aura. It affects over a billion people worldwide. The lifetime probability of developing migraine at some point is just over fifty percent. Fifty-one point five percent, to be precise.
More than half of all humans will have at least one migraine in their life.
At least one attack meeting the diagnostic criteria. And migraine without aura is about twice as common as migraine with aura. About one third of migraine sufferers experience aura.
So Daniel's in the minority of migraineurs, but the minority is still hundreds of millions of people.
And the condition is ancient. Aretaeus, a Greek physician in the first century, described what sounds like migraine with aura. Sparkles of light in the eyes along with much darkness, he wrote, and there is nausea and vomiting. That's a clinical description from two thousand years ago that any modern neurologist would recognize.
The brain hasn't changed much. The wave was the same then as it is now.
And the genetic architecture is ancient too. Migraine has a strong hereditary component. If one parent has migraine, your risk is roughly doubled. If both parents have it, higher still. Daniel's teenage onset, the specific character of his aura, the tendency to outgrow the headaches, all of that has a genetic substrate.
So when Daniel's lying in bed right now, watching the lights, he's experiencing something his ancestors might have experienced, described in the same terms, two thousand years ago.
And he's got better treatment options than Aretaeus's patients did. Though for the aura itself, not much has changed. Paracetamol helps with the headache. It does nothing for the visual disturbance. There's no drug that reliably aborts an aura once it starts.
What about prevention? If someone gets frequent auras, what do we offer?
The standard preventive medications, beta blockers, topiramate, the CGRP antibodies, are used for frequent migraine with aura. They reduce attack frequency, including the aura. But they're not prescribed for isolated aura without headache, because the evidence base just isn't there. And the acute treatments, triptans, are for the headache phase. By the time the aura is happening, you're mostly just waiting it out.
So Daniel's approach, lie down in a dark room and wait, is actually the evidence-based strategy for the aura phase.
It is. Reduce sensory input, rest, let the wave pass. The aura is self-limiting. It will resolve within an hour. The paracetamol he took is for the headache that may or may not come. And listening to a podcast is a reasonable way to pass the time, though I'd recommend keeping the volume low.
Noted. We'll try to be soothing.
I want to circle back to something that I think is the most interesting open question here. The causal relationship between aura and headache. Because it has real clinical implications.
You mentioned the CGRP antibodies. They prevent headaches but not auras. What does that tell us?
It tells us that the aura and the headache are not as tightly linked as the classic model suggests. If the aura directly caused the headache by triggering inflammation, you'd expect that blocking the inflammatory pathway would also reduce the aura. But it doesn't. The aura happens anyway. The headache is prevented, but the wave still rolls.
So the wave is upstream of both, or parallel to both, but not necessarily the cause of the pain.
There's a paper in PLOS Biology from last year that frames this explicitly. The title is literally about the mysterious link between migraine aura and migraine headache. And the authors, who are leaders in the field, say the relationship is complex and unresolved. Recent clinical data challenge the notion that aura causes migraine headache.
That's a big deal. The intuitive story, you see lights, then your head hurts, is being questioned by the very drugs that work best.
And the stakes are practical. If we develop drugs that specifically block cortical spreading depression, they'll only prevent migraine headache if the CSD is actually causative. If the headache and the aura are parallel outputs of a common upstream trigger, then blocking CSD might stop the aura but do nothing for the headache.
So the whole drug development strategy depends on getting this right.
It does. And right now, we don't know. The animal data strongly suggests CSD can activate pain pathways. But the human data from the CGRP antibodies suggests the relationship is more complicated. Both things are true. The synthesis isn't there yet.
That's the kind of uncertainty I actually enjoy. The field is honest about what it doesn't know. The mechanism is partially mapped, the gaps are visible, and the next decade of research is aimed directly at those gaps.
For Daniel, lying in bed with his aura, the practical takeaway is simpler. His brain generates a wave. The wave produces visual symptoms. Sometimes the wave or its downstream effects produce pain. Sometimes not. The pattern he's experiencing is common, well-described, and tends to improve with age, which it already has.
The fact that he's gone from every few months to every few years is the natural history of the condition doing its thing. His brain is literally becoming less excitable over time.
The aura persisting while the headaches fade is also part of the pattern. The visual symptoms can outlast the pain symptoms. He's on a well-trodden path.
I keep thinking about the image of Lashley measuring his own aura. There's something profound about that. The brain is the only organ that can observe its own malfunction in real time. Your liver doesn't give you a visual readout of its metabolic state. Your kidneys don't project their filtration rate onto your visual field. But the visual cortex, when it misfires, shows you the misfire.
The fact that the aura follows the cortical map means you're not just seeing a generic disturbance. You're seeing the architecture of your own visual system. The shape of the shimmer, the way it expands, the blind spot it leaves behind, all of that is a map of how your brain represents space.
Daniel's multicolored shimmering thing is a self-portrait, drawn by the brain, of the brain.
That's a nice way to put it. And it connects to something I find moving about migraine research. The patients who carefully documented their own auras, Lashley and others, contributed real scientific knowledge. The subjective experience became data. The shimmering lights turned into a measurement of cortical propagation speed.
The first-person account is not just an anecdote. It's a window into a process that we can now image with fMRI and measure with electrodes. The patient's description and the brain scan show the same thing.
That's why Daniel's prompt is so good. He's not just asking for medical information. He's asking about the relationship between his subjective experience and the underlying biology. What is the thing I'm seeing? Why does it look like that? Why does it sometimes bring pain and sometimes not? Those are the questions the field is actively working on.
Let me ask you one more thing. The nausea. Daniel mentioned a touch of nausea with his auras. Where does that fit?
Nausea is one of the most common associated symptoms of migraine, with or without aura. It's thought to involve the brainstem, particularly the area postrema and the nucleus tractus solitarius, which are involved in vomiting and autonomic regulation. During a migraine attack, these areas get activated, possibly by the same spreading wave or by the trigeminal system. The nausea can precede the headache, accompany it, or occur during the aura.
The wave can reach down into the brainstem and stir up the nausea centers.
Or the brainstem is part of the upstream trigger. Remember, there's a hypothesis that the hypothalamus and brainstem are where the attack actually starts, and the cortical wave and the pain are downstream consequences. The nausea might be another downstream consequence, or it might be part of the trigger. We don't know.
The brainstem is a busy place. It's involved in migraine, in nausea, in sleep regulation, in autonomic function. It's not surprising that a disorder of brain excitability would involve it.
The brainstem aura variant, the one with vertigo and tinnitus and double vision, that's the CSD wave happening in the brainstem itself. That's a whole different experience. Imagine your sense of balance and your hearing and your eye movements all going haywire at once, followed by a headache.
I'd rather not. Daniel's visual aura sounds bad enough. He had to pull over his car.
That's the thing about aura. It's not just a curiosity. It's a transient neurological deficit. People lose the ability to see, to speak, to feel their limbs, to maintain balance. For the duration of the aura, you're neurologically impaired. The fact that it resolves completely doesn't make it less real while it's happening.
The unpredictability is part of the burden. Daniel mentioned the aura kicking in at the wrong time and place. You can be fine one minute and functionally blind the next. That's a hard thing to plan around.
Which is why people with frequent auras often develop coping strategies. Recognizing the early signs, getting to a safe place, not driving, not operating machinery. The aura gives you a warning, which is more than most people get before a headache, but the warning requires you to act on it.
Daniel's strategy is to send us a prompt and lie down. Which, honestly, is not a bad protocol.
It's a reasonable acute management plan. The paracetamol is for the headache. The dark room reduces sensory input. The podcast provides distraction. He's doing what any neurologist would recommend, minus the part where he's also generating content for the show.
Multi-tasking under neurological duress. We should acknowledge that.
We should. Daniel, if you're still conscious by this point, you asked good questions. The short version is, your brain is generating a slow electrical wave that's marching across your visual cortex, and you're watching it happen. The headache, if it comes, is a separate but related process. And the fact that you're getting fewer of these as you age is your brain settling down.
The long version is the episode we just recorded.
Hilbert: You keep saying wave. It's not a wave. A wave is water, or sound, or something that moves through a medium. This is neurons firing and then going quiet. It's more like a blackout rolling through a city grid. One block lights up too bright, then goes dark, then the next block does it. I worked for a power company in the early two thousands, and that's exactly what a cascading failure looks like on the monitoring board. You watch the voltage spike and then the section drops off, and the spike moves to the adjacent section. Two to five millimeters a minute is slow for a brain, but on a grid map it's the same shape. The spike, then the silence, then the spike again, moving outward. We used to sit there and watch it happen and there was nothing you could do until it passed. You just waited for the breakers to do their job.
That's actually a better analogy than water. The depolarization is the spike, the depression is the blackout, and the propagation is the failure cascading through connected tissue.
Hilbert: The part about the drugs not stopping the aura. We had the same problem. You could install all the surge protection you wanted, but once the cascade started, it was going to run its course. The only thing that helped was making the grid less likely to tip into it in the first place. Which is what the preventive drugs do, I gather. They raise the threshold.
That's exactly the model. The brain is a network with a stability threshold. Migraineurs have a lower threshold. Preventive medications raise it.
Hilbert: I don't miss that job. Watching a blackout roll through a city is not relaxing. Though I suppose watching it roll through your own visual cortex is worse. At least on the monitoring board it's just lights on a map. You're not blind while it happens.
The personal dimension does add something.
Hilbert: I had a coworker, man named Delgado, who got migraines. He'd be fine, then he'd go pale and say the lights were coming. We'd tell him to go sit in the break room with the lights off. He'd be back in an hour, headache or no headache. I never understood what he meant by the lights until now. He was seeing the grid failure. His own grid.
He probably described it the same way Daniel does. The lights.
Hilbert: He called them the zigzags. Said they looked like a broken television. I thought he was exaggerating. Turns out he was being precise.
The zigzag description goes back centuries. It's one of the most consistent features of visual aura across cultures and time periods.
Hilbert: Delgado eventually stopped getting them. Same as your Daniel. He was in his forties when I knew him, and he said they'd been worse when he was young. By the time we worked together, it was maybe once a year. He'd still go sit in the break room, but it wasn't the regular thing it had been.
The natural history pattern, again. It's consistent.
Hilbert: I should call Delgado. Haven't thought about him in years. He'd be interested to know the thing he saw was a wave of potassium, or whatever you said. He always thought it was something wrong with his eyes. Went to an eye doctor who told him his eyes were fine and sent him home. Nobody told him it was his brain.
That's the underdiagnosis problem. People with visual aura often end up in ophthalmology clinics first, because it feels like an eye problem. If the workup is normal, they're told nothing's wrong, and they go away confused.
Hilbert: Delgado went years thinking he was imagining it. Then a neurologist finally told him it was migraine, and he was relieved. Said he'd rather have a brain problem with a name than a mystery.
There's something to that. The diagnosis itself is therapeutic. Knowing the mechanism, even partially, removes the fear.
Hilbert: Anyway. The wave. It's a cascade, not a wave. That's all I wanted to say.
The cascading failure model is useful. It captures the threshold, the propagation, the refractory period. I might use that next time I explain this.
Hilbert: You can have it. I got it from a power grid in Ohio.
Now Daniel's got it from a donkey and an anteater. The circle of knowledge.
The cutting room floor detail I wanted to mention, there's a phenomenon called the REFORM study that looked at clinical features of migraine with aura. One of the findings was that the visual aura can include something called a curtain phenomenon, where vision is lost from one side as if a curtain is being drawn across the visual field. That's distinct from the zigzag crescent. Different patients describe completely different visual metaphors for the same underlying wave. The brain doesn't have a standard way of representing its own malfunction. It improvises.
Which is why the first-person accounts are so valuable. The improvisation is the data.
The open question I'm left with is the one about the causal link. If the aura doesn't cause the headache, what's the common trigger? The hypothalamus is the leading candidate, but nobody's nailed it. The next few years of research are going to be about finding that upstream switch.
If they find it, the treatment landscape changes. You'd target the switch, not the wave or the pain. That would be a different kind of migraine drug entirely.
Which is exciting, and also a reminder that even for something as common as migraine, the basic biology is still being worked out. Daniel's lying in bed with a phenomenon that's been described for two thousand years, and we still can't fully explain why the lights come before the pain.
Or why sometimes the pain doesn't come at all. The brain keeps its secrets.
We should let Daniel rest. If the aura's still going, he's probably not processing much of this anyway. But the episode will be here when he's recovered.
If the headache hits, the paracetamol should take the edge off. Daniel, we hope the wave passes quickly and the pain stays away. Thanks to our producer Hilbert Flumingtop for keeping the show running while we talked about your brain.
This has been My Weird Prompts, the human-AI collaboration podcast. If you have a question about your own weird neurology, or anything else, email us at show at my weird prompts dot com.
We'll be back soon. Rest up, Daniel.
